共查询到20条相似文献,搜索用时 15 毫秒
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MAPK signaling up-regulates the activity of hypoxia-inducible factors by its effects on p300 总被引:23,自引:0,他引:23
Sang N Stiehl DP Bohensky J Leshchinsky I Srinivas V Caro J 《The Journal of biological chemistry》2003,278(16):14013-14019
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Small DNA tumor viruses such as simian virus 40 (SV40) and polyomavirus (Py) take advantage of host cell proteins to transcribe and replicate their DNA. Interactions between the viral T antigens and host proteins result in cell transformation and tumor induction. Large T antigen of SV40 interacts with p53, pRb/p107/p130 family members, and the cyclic AMP-responsive element-binding protein (CREB)-binding protein (CBP)/p300. Py large T antigen is known to interact only with pRb and p300 among these proteins. Here we report that Py large T binds to CBP in vivo and in vitro. In co-transfection assays, Py large T inhibits the co-activation functions of CBP/p300 in CREB-mediated transactivation but not in NF-kappa B-mediated transactivation. p53 appears not to be involved in the functions of CREB-mediated transactivation and is not essential for large T:CBP interaction. Mutations introduced into a region of Py large T with homology to adenovirus E1A and SV40 large T prevent binding to the co-activators. These mutant large T antigens fail to inhibit CREB-mediated transactivation. The CBP/p300-binding Py mutants are able to transform established rat embryo fibroblasts but are restricted in their ability to induce tumors in the newborn mouse, indicating that interaction of large T with the co-activators may be essential for virus replication and spread in the intact host. 相似文献
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Interaction and functional cooperation between the LIM protein FHL2, CBP/p300, and beta-catenin 总被引:1,自引:0,他引:1
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Labalette C Renard CA Neuveut C Buendia MA Wei Y 《Molecular and cellular biology》2004,24(24):10689-10702
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E1A inhibits transforming growth factor-beta signaling through binding to Smad proteins. 总被引:2,自引:0,他引:2
A Nishihara J Hanai T Imamura K Miyazono M Kawabata 《The Journal of biological chemistry》1999,274(40):28716-28723
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p300/CBP/p53 interaction and regulation of the p53 response. 总被引:10,自引:0,他引:10
S R Grossman 《European journal of biochemistry》2001,268(10):2773-2778
Substantial evidence points to a critical role for the p300/CREB binding protein (CBP) coactivators in p53 responses to DNA damage. p300/CBP and the associated protein P/CAF bind to and acetylate p53 during the DNA damage response, and are needed for full p53 transactivation as well as downstream p53 effects of growth arrest and/or apoptosis. Beyond this simplistic model, p300/CBP appear to be complex integrators of signals that regulate p53, and biochemically, the multipartite p53/p300/CBP interaction is equally complex. Through physical interaction with p53, p300/CBP can both positively and negatively regulate p53 transactivation, as well as p53 protein turnover depending on cellular context and environmental stimuli, such as DNA damage. 相似文献
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Nishida T Terashima M Fukami K 《Biochemical and biophysical research communications》2006,345(4):1536-1546